IDENTIFICATION OF BIOMARKERS FOR EARLY TENDON DEGENERATION USING AN IN-VIVO RABBIT MODEL

Introduction Tendinopathy is a common and costly diagnosis in workers with Activity-related Soft Tissue Disorder (ASTD), and in recreational and professional athletes. The associated pain results in reduced physical activity, reduced productivity, missed work days, and substantial costs to the government. Workers whose tendons are exposed to prolonged repetitive activity (eg, manual workers like fish processors) and/or high mechanical loads (eg, construction workers) are at high risk for the development of ASTD-associated tendinopathy. Pain is usually one of the first symptoms of tendinopathy; however imaging studies have demonstrated that significant degenerative tendon alterations can develop in response to mechanical loading, months before there are any overt symptoms. Goal: To identify circulation markers of early tendon degeneration. Research questions: (1) Will fatigue damage in tendons, caused by different loading regimes, correlate with changes in expression of genes involved in tendon degeneration? (2) Can we track the development of early phase tendon degeneration in vivo using ultrasound and measure indicators of tendon degradative activity in the circulation? It is hypothesised that different loading regimes will lead to characteristic, degradative differences in gene expression. Ultrasound will be able to visualise and follow early onset, degradative changes in the strained tendons. Methods Rabbit Achilles tendons will be subjected to varying loading regimens using the in-vivo Backman model. After set periods of exercise, microdialysis and blood samples will be taken and analysed for genes involved in degradation of tendons. At the same intervals, ultrasound images will be taken to track changes in the cross sectional area of the tendon. After the end of the full exercise period, the tendon tissue will be examined for characteristic degradative changes using microscopy. Results It is expected that the exercise regimen will lead to significant changes in gene expression in the tendon.1 Blood and microdialysis samples are expected to show significant changes in for example, collagen type I and III, matrix metalloproteinases (MMPs), tissue inhibitors for MMPs (TIMPs), and other genes involved.2 It is expected that the tissue will exhibit characteristic morphological changes seen in degradative tendon tissue, for example, rounded nuclei of tenocytes and a looser, kinked pattern of the collagen fibrils.3 Discussion Treatment for tendinopathies in workers can be a long and costly process which is not always successful, due to the degenerative nature of chronic tendinopathy. Detecting the early stages of tendinopathy could allow for the possibility of interventions to decrease or prevent tendon pain and/or rupture, and reduce healthcare and insurance costs.

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